Effect of methamphetamine on ultraweak photon emission and level of reactive oxygen species in male rat brain. (28th March 2023)

• Record Type: Journal Article
• Authors: Esmaeilpour, Tahereh; Lotfealian, Azam; Anvari, Morteza; Namavar, Mohammadreza; Karbalaei, Narges; Shahedi, Abbas; Bokkon, Istvan; Salari, Vahid; Oblak, Daniel
• Is Part Of: Neuroscience letters. Volume 801(2023)
• Publication Date: 2023-03-28
• Subjects: Ultraweak Photon Emission -- Reactive Oxygen Species -- Methamphetamine -- Mitochondria -- Brain; Neurology -- Periodicals; Neurology -- Periodicals; Research -- Periodicals; Neurologie -- Périodiques; Neuroanatomie -- Périodiques; Neuropharmacologie -- Périodiques; Neurophysiologie -- Périodiques; Neurology; Periodicals; Electronic journals; 617.48
• DOI: 10.1016/j.neulet.2023.137136
• Languages: English
• ISSNs: 0304-3940

Abstract

Graphical abstract: Highlights: Methamphetamine (METH) increases ultraweak photon emission (UPE) and reactive oxygen species (ROS) in the prefrontal, motor, and visual regions. UPE may be used as a potential dynamic reading tool in METH research to monitor oxidative metabolism in physiological processes related to ROS. Abstract: All living cells, including neurons, generate ultra-weak photon emission (UPE) during biological activity, and in particular, in the brain, it has been shown that UPE is correlated with neuronal activity and associated metabolic processes. Various intracellular factors, as well as external factors, can reduce or increase the intensity of UPE. In this study, we have used Methamphetamine (METH) as one potentially effective external factor, which is a substance that has the property of stimulating the central nervous system. METH can impair mitochondrial function by causing toxicity via various pathways, including an increase in the number of mitochondria, hyperthermia, the increased metabolic activity of the brain, and the production of glutamate and excess calcium. In addition to mitochondrial dysfunction, METH alters cellular homeostasis, leading to cell damage and the production of excess ROS. The aim of this study is to measure and compare the UPE intensity and reactive oxygen species (ROS) levels of the prefrontal, motor, and visual cortex before and after METH administration. Twenty male rats were randomly assigned to two groups, the control, and METH groups. In the control group, 2 h after injection of normal saline and without any intervention, and in the experimental group 2 h after IP injection of 20 mg/kg METH, sections were prepared from three areas: prefrontal, motor, and V1-V2 cortex, which were used to evaluate the emission of UPE using a photomultiplier tube (PMT) device and to evaluate the amount of ROS. The results showed that the amount of ROS and UPE in the experimental group in all three areas significantly increased compared to the control group. So, METH increases UPE and ROS in the prefrontal, motor, and visual regions, and there is a direct relationship between UPE intensity and ROS production. Therefore, UPE may be used as a dynamic reading tool to monitor oxidative metabolism in physiological processes related to ROS and METH research. Also, the results of this experiment may create a new avenue to test the hypothesis that the excess in UPE generation may lead to the phenomenon of phosphene and visual hallucinations.